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Although rare in man, in other species, genetically determined autoimmunity can be demonstrated. Similar diseases have been observed in man and in animals and it is suggested that common mechanisms may underlie these observations. A decreased ability to generate suppressor and effector T cells are characteristics of genetically predetermined autoimmunity. A similar cell mediated immune abnormality is seen in patients with chronic inflammatory disease. One of the first cells encountered in the tissues involved in this disease is the macrophage. Once activated, the macrophage is primed to produce bioreactive substances and can become immunologically activated by adherence to an endothelial surface. These activated macrophages may become programmed to produce an inflammatory response in the tissue by the secretion of various bioreactive substances. In this fashion, a local reaction is induced in the tissues and a primary inflammatory response is initiated. The inflammatory process may be orchestrated by mediators such as lymphokines and eicosanoids. This mechanism may be responsible for the chronic inflammatory response seen in a variety of diseases.Endoplasmic reticulum stress and autophagy as novel targets for treatment of vascular inflammation.
Endoplasmic reticulum (ER) stress is an adaptive response to unfolded protein accumulation in the ER that activates the unfolded protein response (UPR) in the cell. Three major branches of UPR are activated; i) PERK (double-stranded RNA-activated protein